Neurological Stressors III Chronic Neurological Disorders: Joy Borrero, RN, MSN and NUR240 Nursing Students

Neurological Stressors III Chronic Neurological Disorders
Joy Borrero, RN, MSN And NUR240 Nursing Students

12/11
Topics
Multiple Sclerosis Amyotropic Lateral Sclerosis (ALS) Parkinsons Disease Myasthenia Gravis Guillain-Barre Syndrome Huntingtons Disease
Chronic Neuromuscular Dysfunction

Some commonalities in adaptations are: Altered motor activity Altered coordination Altered sensory function Altered urinary/bowel patterns Altered role/self perception Altered speech/swallowing Impaired physical mobility Risk for injury Nutrition less than body requirements Risk for aspiration
Multiple Sclerosis (MS)

Etiology: Types: S&S: Dx: Triggers: Tx:
Multiple Sclerosis
Chronic autoimmune disease affecting the myelin sheath and conduction pathway of the CNS Characterized by periods of remission and exacerbation Inflammatory response resulting in random or patchy areas of plaque in the white matter of the CNS Demyelination of brain and spinal cord, affects conduction pathway of CNS Two major courses: relapsing and remitting, and chronic and progressive
Multiple Sclerosis (MS)

Exact cause unknown, may be defective immune response, early viral infection. More common in people living in northern temperate climate. Affects twice as many women than men. Typically occurs between ages 20-40 Family hx of MS in 15% of cases No cure for the disease Dx- McDonald criteria http://www.nmss.org/
MS
Primary Symptoms: Fatigue, weakness, numbness Difficulty in coordination, loss of balance Visual disturbances: blurring, diplopia, patchy or total blindness, change in peripheral vision, nystagmus Speech defects Dysarthria, dysphagia Spastic weakness, ataxia, tremors, dysmetria Emotional lability, depression/euphoria. Bladder/bowel dysfunction Tinnitus, vertigo, decreasing hearing acuity Cognitive changes-memory loss, impaired judgement
MS
Secondary symptomsProblems/complications that occur a/r/o primary symptoms Repeated UTIs Loss of muscle tone and disuse weakness Poor posture and control of torso Decreased bone density Shallow inefficient breathing Pressure ulcers from immobility
Pharmacology
Biological response modifiers- Inteferon Monoclonal antibody- Natalizumab Synthetic protein-Glatiramer acetate Immunosuppressives-Cyclosporine Corticosteroids-Prednisone Antispasmodic drugs-Dantrolene, Baclofen Anticonvulsants-Dilantin Stool softeners-Colace Anticholinergics-Probanthine Beta-blockers- Inderal (tremors) CAM Therapy
Biological Response Modifiers

Interferon Betaseron- blocks replication of viruses and stimulates host immunoregulatory activities. Reduce frequency of exacerbations Dose 0.25 mg sc every other day. Adverse effects: Dizziness, confusion, anorexia, hypotension, leukopenia, flu like symptoms, depression,suicidal ideation Thrombocytopenia
Amytropic Lateral Sclerosis ALS

Amyotrophic Lateral Sclerosis (ALS)

Deteriorating disease of motor neurons in anterior horn of spinal cord and motor nuclei of lower brain stem AKA Lou Gehrigs disease Etiology unknown. More common men 50-60. Manifestations: Depends on location of affected motor neurons, atrophy and twitching. Death occurs within 2-5 years after onset of symptoms.
Diagnostic Procedures
Creatine kinase (CK)- increased Electromyography (EMG)- Muscle fasciculations http://www.youtube.com/watch?v=k0uSpYd_I cs Muscle biopsy- Muscle atrophy Serial muscle testing- Loss of muscle strength Pulmonary function tests
Assessments & Interventions

Assess airway, resp status Assess speech patterns, skin integrity No known cure, no treatment, no preventive measures Riluzole, only drug approved by FDA to extend survival time Exercise and mobility program Management of swallowing difficulties
Interventions
Teach swallowing technique Maintain resp. function- assess lung sounds,suction prn, C&DB Administer Quinine for muscle cramps Antispasmotics: baclofen, dantrolene, diazepam www.als.org for pt/family support and education
Parkinsons Disease
Parkinsons disease
Cause unknown-progressively debilitating disease that affects gross motor function. Degeneration of the nerves that control voluntary movement. Occurs in the part of the brain called the substantia nigra Neurons here communicate with other neurons in the brain using a neurotransmitter called dopamine. When these neurons that make dopamine die, signaling between neurons is severely hampered, causing a loss of controlled movement Risk factors Dx Procedures
Manifestations
Manifestations:
Stooped posture, postural instability, head bent forward Tremors of head and hand, pill rolling Akinesia, Bradykinesia Rigid stance, shuffling and propulsive gait Mask like facial expression
Parkinsons disease
Impaired physical mobility r/t muscle rigidity and weakness. Self care deficit r/t to tremor and motor disturbance. Risk for falls Risk for imbalanced nutrition: Less than body requirements, r/t tremor, slowness in eating, difficulty in chewing and swallowing.
Drug Therapy for Parkinsons Goal: Increase patients functional abilities

Levodopa
Anticholinergics :
Cogentin
COMT Inhibitors
PD Meds
Dopamine Agonists: Mirapex
Amantadine: Symmetrel
MAOI: Eledepryl
Parkinsons disease
levodopa (Dopar, Laradopa)- antiparkinson agent, precursor of dopamine that can cross the blood brain barrier, then is transformed to dopamine. levodopa and carbidopa (Sinemet)- GOLD STANDARD,antiparkinsonian combo meddosage is adjusted to patients symptoms Adverse effects involuntary movements, ataxia, increased tremor, anorexia
Parkinsons disease
Amantadine hydrochloride (Symmetrel) Antiviral and Antiparkinsonian Therapeutic actions thought to increase dopamine release, helpful in treating bradykinesia, rigidity and tremor. Dose 100 mg po bid (up to 400 mg) Adverse- dizziness, insomnia, dry mouth, confusion, constipation, urinary retention, orthostatic hypotension.
Parkinsons Disease
Complications: Aspiration pneumonia Altered cognition, dementia
Additional therapeutic options: Thalamotomy Stereotactic Pallidotomy Deep Brain Stimulation

http://www.parkinsons.org
Myasthenia Gravis
Myasthenia Gravis
Progressive autoimmune disease resulting in severe muscle weakness. Women 15-35 or men over 40. Exacerbations and remissions Manifestations: Extreme muscle weakness and fatiguability. Diplopia and ptosis are early signs Sleepy, mask like expression, dysphonia. Problems chewing and swallowing aspiration Progressive weakness of diaphragm- resp. distress.
Myasthenia Gravis
Diagnostic tests pt. history and exam, Tensilon testing IV tensilon relieves symptoms within 30 seconds. Positive result. AChR-Acetylcholine receptor antibodies found serum of 90%. EMG- shows neuromuscular transmission characteristics.
Therapeutic Procedures
Plasmapheresis Thymectomy
http://www.myasthenia.org
Medications
Anticholinesterase meds- pyridostigmine (Mestinon) and ambenonium (Mytelase) Administer with small amount of food to avoid GI upset and eat within 45 minutes. Must be administerd on time and same time each day. Potential SE is cholinergic crisis Cotricosteroids Immunosuppressants
Complications
Myasthenic Crisis Undermedication
Resp muscle weaknessmechanical ventilation Myasthenic symptomsweakness, incontinence,fatigue Hypertension Temp improvement of symptoms with Tensilon
Cholinergic Crisis Overmedication

Muscle twitching results in resp muscle weakness, mech ventilation Cholinergic symptomshypersecretions,hypermotility Hypotension Tensilon has no positive effect on symptoms Symptoms improve with anticholinergic meds
Guillain-Barre Syndrome
Etiology: Types: S&S: Dx: Tx:
Guillian Barre Syndrome

Acute inflammatory disease of unknown origin Usually preceeded by a viral infection (URI or GI) 1-4 weeks Degeneration of the myelin sheath of peripheral nerves Manifestations: paresthesias, ascending weakness in legs progresses to paralysis,autonomic dysfunction Diagnosis by H&P, CSF exam.
Facts
Most people reach the stage of greatest weakness within 2 weeks after symptoms appear, and by the 3rd week 90% of all patients are at their weakest. Recovery may be from a few weeks to a few years 30% will have residual weakness after 3yrs 3% may suffer a relapse
Huntingtons Disease
Etiology: S&S: Dx: Tx:
MANAGEMENT
Dx: made on basis of symptoms and family hx Genetic counseling and testing Tx: Haldol and Navane Riluzole Antidepressants

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Neurological Stressors III Chronic Neurological Disorders

Joy Borrero, RN, MSN And NUR240 Nursing Students

Chronic Neuromuscular Dysfunction

Multiple Sclerosis (MS)

Multiple Sclerosis (MS)

Biological Response Modifiers

Amytropic Lateral Sclerosis ALS

Amyotrophic Lateral Sclerosis (ALS)

Assessments & Interventions

Drug Therapy for Parkinsons Goal: Increase patients functional abilities

Additional therapeutic options: Thalamotomy Stereotactic Pallidotomy Deep Brain Stimulation

Cholinergic Crisis Overmedication

Guillian Barre Syndrome

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